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骨骼肌衰老的代谢组学分析。

Metabolomic Analysis of Skeletal Muscle in Aged Mice.

机构信息

Graduate School of Life and Environmental Sciences, Kyoto Prefectural University, Kyoto, Japan.

Laboratories of Nutritional Biochemistry, Graduate School of Nutritional and Environmental Sciences, University of Shizuoka, Shizuoka, Japan.

出版信息

Sci Rep. 2019 Jul 18;9(1):10425. doi: 10.1038/s41598-019-46929-8.

DOI:10.1038/s41598-019-46929-8
PMID:31320689
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6639307/
Abstract

Sarcopenia is the age-induced, progressive loss of skeletal muscle mass and function. To better understand changes in skeletal muscle during sarcopenia, we performed a metabolomic analysis of skeletal muscle in young (8-week-old) and aged (28-month-old) mice by using capillary electrophoresis with electrospray ionization time-of-flight mass spectrometry. Principal component analysis showed clear changes in metabolites between young and aged mice. Glucose metabolism products were decreased in aged mice, specifically fructose 1,6-diphosphate (0.4-fold) and dihydroxyacetone phosphate (0.6-fold), possibly from decreased glycolytic muscle fibers. Multiple metabolic products associated with phospholipid metabolism were significantly changed in aged mice, which may reflect changes in cell membrane phospholipids of skeletal muscle. Products of polyamine metabolism, which are known to increase nucleic acid and protein synthesis, decreased in spermine (0.5-fold) and spermidine (0.6-fold) levels. By contrast, neurotransmitter levels were increased in skeletal muscle of aged mice, including acetylcholine (1.8-fold), histamine (2.6-fold), and serotonin (1.7-fold). The increase in acetylcholine might compensate for age-associated dropout of neuromuscular junctions, whereas the increases in histamine and serotonin might be due to muscle injury associated with aging. Further analysis focusing on the altered metabolites observed in this study will provide essential data for understanding aging muscles.

摘要

肌肉减少症是一种与年龄相关的、进行性的骨骼肌质量和功能丧失。为了更好地了解肌肉减少症过程中骨骼肌的变化,我们采用毛细管电泳-电喷雾电离飞行时间质谱联用技术对年轻(8 周龄)和年老(28 月龄)小鼠的骨骼肌进行了代谢组学分析。主成分分析显示,年轻和年老小鼠之间的代谢物有明显变化。年老小鼠的葡萄糖代谢产物减少,具体表现为 1,6-二磷酸果糖(减少 0.4 倍)和二羟丙酮磷酸(减少 0.6 倍),可能是由于糖酵解肌纤维减少所致。与磷脂代谢相关的多种代谢产物在年老小鼠中发生了显著变化,这可能反映了骨骼肌细胞膜磷脂的变化。多胺代谢产物与核酸和蛋白质合成增加有关,其中精脒(减少 0.5 倍)和精胺(减少 0.6 倍)水平降低。相比之下,年老小鼠骨骼肌中的神经递质水平增加,包括乙酰胆碱(增加 1.8 倍)、组胺(增加 2.6 倍)和 5-羟色胺(增加 1.7 倍)。乙酰胆碱的增加可能补偿了与年龄相关的神经肌肉接头丢失,而组胺和 5-羟色胺的增加可能是由于与衰老相关的肌肉损伤所致。进一步分析本研究中观察到的改变的代谢物将为了解衰老肌肉提供重要数据。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/60c2/6639307/22f020b50791/41598_2019_46929_Fig8_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/60c2/6639307/fcc25c78ecdf/41598_2019_46929_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/60c2/6639307/da984d87c4d7/41598_2019_46929_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/60c2/6639307/ac753457e69c/41598_2019_46929_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/60c2/6639307/6fe966cdb3ff/41598_2019_46929_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/60c2/6639307/e5f9627674ef/41598_2019_46929_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/60c2/6639307/6c2ab9a76d74/41598_2019_46929_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/60c2/6639307/f9e4e88d0f83/41598_2019_46929_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/60c2/6639307/22f020b50791/41598_2019_46929_Fig8_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/60c2/6639307/fcc25c78ecdf/41598_2019_46929_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/60c2/6639307/da984d87c4d7/41598_2019_46929_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/60c2/6639307/ac753457e69c/41598_2019_46929_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/60c2/6639307/6fe966cdb3ff/41598_2019_46929_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/60c2/6639307/e5f9627674ef/41598_2019_46929_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/60c2/6639307/6c2ab9a76d74/41598_2019_46929_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/60c2/6639307/f9e4e88d0f83/41598_2019_46929_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/60c2/6639307/22f020b50791/41598_2019_46929_Fig8_HTML.jpg

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